Increased levels of tissue plasminogen activator (t-PA) and tissue plasminogen activator inhibitor (PAI) correlate with tumor necrosis factor alpha (TNFα)-release in patients suffering from microangiopathy following allogeneic bone marrow transplantation (BMT)

Ch Seeber, E. Hiller, E. Holler, H. J. Kolb

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34 Scopus citations

Abstract

Severe microangiopathy resembling thrombotic thrombocytopenic purpura (TTP) has been reported as a complication of acute graft-versus-host disease (aGvHD) in patients receiving Ciclosporin (CsA) prophylaxis following allogeneic BMT. In order to analyze the pathophysiological events involved in microangiopathy, a prospective study comparing release of von Williebrand Factor (vWF), t-PA and PAI, as well as TNFα and further coagulation parameters was performed in 32 patients. Endothelial damage as the central lesion was confirmed by the close association of vWF and t-PA:Antigen with severity of microangiopathy. t-PA activity, however, was neutralized by a simultaneous rise in PAI. Activation of coagulation in the course of microangiopathy was further confirmed by increased levels of DDimer (DDi), fibrinopeptide A (FPA), β-thromboglobulin (βTG) and platelet factor 4 (PF4). As clinical grades of microangiopathy, as well as the release of t-PA:Ag and PAI were correlated with systemic release of TNFα our data further support our hypothesis of cytokine induced endothelial damage in clinical complications following allogeneic BMT.

Original languageEnglish
Pages (from-to)373-383
Number of pages11
JournalThrombosis Research
Volume66
Issue number4
DOIs
StatePublished - 15 May 1992
Externally publishedYes

Keywords

  • bone marrow transplantation
  • microangiopathy
  • plasminogen activator inhibitor 1
  • tissue plasminogen activator
  • tumor necrosis factor α
  • von Willebrand factor

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